Epstein-Barr virus is a unique, ubiquitous, herpesvirus that infects B-- lymphocytes and epithelial cells. in humans. infection of B-lymphocytes results in immortalization of a proportion of the cells, while infection of epithelial cells results in virus replication. Much evidence has been accumulated to suggest that infection of B-lymphocytes in vivo is responsible for virus latency. The precise cell-virus interaction occurring in the circulating B cells remains undefined, but it is clear that B-lymphocytes latently infected with EBV in vivo can generate spontaneously continuous cell lines, infected with EBV, when cultured in-vitro. This raises the question of how B cells latently infected with EBV in vivo fail to expand in vivo. Several mechanisms have been prepared, most of which are immunologic in nature. We have studied in detail suppression, one such immunoregulatory function. In particular, we have been able to generate a suppressor T cell line from an EBV seropositive individual that inhibits the growth of EBV-infected B-cells. This cell line expresses the surface determinant CD8, a marker for suppressor cytotoxic T cells, but has no cytotoxic activity. Rather, it displays an antiproliferative effect exerted upon B-cells' growth stimulated by EBV. We have begun to analyze the mechanism of action of such suppressor T cells, and found that these suppressor cells absorb/use preferentially the growth factors required by the EBV-immortalized B-cells for growth. Thus, suppressor T-lymphocytes regulate the growth of EBV-immortalized B cells by depriving the culture medium of autocrine growth factors produced by the EBV-immortalized B cells which are required for B cell growth.